Mouse outer hair cells lacking the alpha9 ACh receptor are motile.

Efferent nerve fibers form chemical synapses at the bases of outer hair cells (OHC), with acetylcholine (ACh) being their principal neurotransmitter. The activation of ACh receptors on OHCs is known to influence cochlear function. These efferent effects exhibit an unusual pharmacology and are generally known to be inhibitory. Recent evidence suggests that an ACh receptor subunit, known as alpha9, plays a dominant role in mediating the olivocochlear neurotransmission to OHCs. In this investigation, we attempt to determine the possible role(s) of the alpha9 subunit in regulating OHC function by examining OHC electromotility and compound action potentials (CAP) in mice carrying a null mutation for the alpha9 gene. Results indicate that cochlear sensitivity, based on CAP thresholds, is similar for homozygous mutant and wild-type mice. Electromotility is also present in OHCs, independent of whether the alpha9 subunit is present or absent.